Nighttime Home Blood Pressure Research Articles

Night-time home versus ambulatory blood pressure in determining target organ damage

This study aimed to evaluate the association of night-time blood pressure (BP) assessed by home blood pressure (HBP) or ambulatory blood pressure (ABP) monitoring with preclinical target organ damage in untreated hypertension. Untreated hypertensive study participants were evaluated with ABP monitoring (24-h) and HBP monitoring during daytime (6 days, duplicate morning and evening measurements) and night-time (automated asleep measurements, three nights, 3-hourly measurements/night). Target organ damage was assessed by echocardiographic left ventricular mass index (LVMI), common carotid intima-media thickness (cIMT), urine albumin excretion (UAE), and ankle-brachial index (ABI). A total of 131 study participants were analysed [mean age 52.1 ± 11.9 (SD) years, BMI 29.9 ± 5.3 kg/m2, men 58%, cardiovascular disease history 6.1%]. Daytime and night-time HBP were slightly higher than the respective ABP values (mean difference for systolic daytime/night-time 3.5 ± 10.6/2.6 ± 9.8 mmHg, P < 0.01 for both comparisons and diastolic -0.3 ± 6.8/1.2 ± 6.2 mmHg, P = NS/0.02, respectively). There was a strong correlation between daytime ABP and HBP (r = 0.71/0.72, systolic/diastolic), as well as between the respective night-time values (r = 0.80/0.79; all P < 0.01). Night-time ABP and HBP presented strong and comparable correlations with all the indices of preclinical target organ damage. In multivariate analyses, both LVMI (R2 = 0.26) and cIMT (R2 = 0.25) were determined by night-time systolic HBP, age and male sex; UAE (R2 = 0.28) by night-time systolic HBP and male sex; ABI (R2 = 0.20) by male sex and night-time home pulse pressure. In untreated hypertensives, night-time BP assessed by home monitoring appears to be as good as night-time ambulatory monitoring in determining preclinical target organ damage.

Assessment of the reductions in night-time blood pressure and dipping induced by antihypertensive medication using a home blood pressure monitor

Night-time blood pressure (BP) is strongly associated with hypertensive target organ damage; however, no previous studies have compared home BP monitor measurements of the reduction in night-time BP induced by antihypertensive medications with those obtained with ambulatory BP monitors. As part of the Japan Morning Surge-Target Organ Protection study, in which candesartan (thiazide diuretics were added, if needed) was administered to hypertensive patients in the morning or at bedtime, 50 hypertensive patients had their night-time home and ambulatory BP successfully measured at the baseline and 6 months. In addition, three night-time home BP readings were taken during sleeping hours (at 2, 3, and 4 o'clock) for 6 months. The mean reduction in night-time BP did not differ significantly between home and ambulatory BP monitoring (10.4 ± 17.9/6.0 ± 12.0 vs. 13.3 ± 14.6/7.6 ± 8.9 mmHg, P = 0.219/0.344), but the differences varied among individual patients. The reduction in night-time BP according to home BP monitoring was significantly correlated with the value obtained with ambulatory BP monitoring (r = 0.51/0.38, P < 0.001/=0.006). The reduction in night-time SBP according to home BP monitoring was significantly correlated with the reductions in left ventricular mass index (r = 0.385, P = 0.013, N = 41) and Sokolow-Lyon voltage (r = 0.335, P = 0.035, N = 40). Home BP monitoring produces estimates of mean night-time BP reductions comparable to those from ambulatory monitoring, while the differences varied among individual patients. The reduction in night-time home BP according to home BP monitoring is significantly correlated with the reduction in left ventricular hypertrophy.

Nighttime Home Blood Pressure and the Risk of Hypertensive Target Organ Damage

In ambulatory blood pressure (BP) monitoring, nighttime BP has a superior ability to predict hypertensive target organ damage than awake BP. We evaluated whether nighttime BP, assessed by a home BP monitor, was associated with hypertensive target organ damage. We measured clinic BP, out-of-clinic BP including nighttime home BP, and the urinary albumin:creatinine ratio (UACR) in 854 patients who had cardiovascular risk factors. Nighttime home BP was measured at 2:00, 3:00, and 4:00 am, in addition to clinic, awake ambulatory, nighttime ambulatory, and awake home BP. Nighttime home systolic BP (SBP) was slightly higher than nighttime ambulatory SBP (difference, 2.6 mm Hg; P<0.001). Clinic (r=0.186), awake ambulatory (r=0.173), nighttime ambulatory (r=0.194), awake home (r=0.298), and nighttime home (r=0.311) SBPs were all associated with log-transformed UACR (all P<0.001). The correlation coefficient for the relationship between nighttime home SBP and log-transformed UACR was significantly greater than that for the relationship between nighttime ambulatory SBP and log-transformed UACR (P<0.001). The goodness of fit of the association between SBP and UACR was improved by adding nighttime home SBP to the other SBPs (P<0.001). Nighttime home diastolic BP also improved the goodness-of-fit of the association between diastolic BP and UACR (P=0.001). Similar findings were observed for the left ventricular mass index in the subgroup (N=594). In conclusion, nighttime home BP is slightly different from (but comparable to) nighttime ambulatory BP. The addition of nighttime home BP to other BP measures improves the association of BP with hypertensive target organ damage.

Kidney and Circadian Blood Pressure Rhythm

Association between nondipper pattern of circadian rhythm of blood pressure (BP) and impaired renal capacity to excrete sodium into urine was confirmed by Bankir et al1 in this issue of Hypertension based on a large number of subjects. Although this association has been observed in small studies,2,3 their study1 is the first to show it in a large-scale setting, and, therefore, is highly welcomed. Because there is a tight link between kidney and hypertension, renal dysfunction causes hypertension, whereas hypertension accelerates renal damage. It is well appreciated that the kidneys play an important role in the long-term regulation of BP. Usually it takes almost 1 week for kidneys to achieve a new steady-state balance of sodium, when sodium intake is altered. Therefore, renal participation in the short-term BP regulation, such as circadian rhythm, has been overlooked. However, the findings of Bankir et al1 strongly suggest that nocturnal hypertension and nondipper pattern of circadian BP rhythm are because of impaired renal capacity to excrete sodium, and circadian BP rhythm is at least in part regulated by kidneys. Sodium sensitivity of BP is also determined by renal capacity to excrete sodium and is regulated by glomerulotubular balance between glomerular ultrafiltration capability and rate of tubular sodium reabsorption.4 Thus, sodium sensitivity is increased in chronic kidney disease (CKD) where glomerular filtration rate (GFR) is reduced and also in disorders with enhanced tubular sodium reabsorption, including primary aldosteronism, diabetes mellitus, and metabolic syndrome, where GFR is augmented. When sodium sensitivity is increased, glomerular capillary pressure is usually elevated, resulting in albuminuria and renal damage. It becomes evident that, in patients with high-sodium sensitivity, the nocturnal dip in …